Ethanol for injection (20% v/v) was prepared by diluting 95% ethanol in 0.9% saline. All ethanol drinking solutions (v/v) were prepared by diluting 95% ethanol (Pharmco Products Inc., Brookfield, CT, USA) with tap water. The MEK1/2 inhibitor SL327 and the p38 inhibitor SB239063 (Tocris Bioscience; Ellisville, MO, USA) were freshly suspended in 45% β-cyclodextrin on the morning of each drug testing day.
Sb239063
Manufactured by Bio-Techne
Sourced in United States
SB239063 is a small molecule inhibitor that targets the p38 mitogen-activated protein kinase (p38 MAPK) pathway. It functions by inhibiting the activity of p38 MAPK, which is involved in various cellular processes, including inflammation, cell proliferation, and apoptosis.
Automatically generated - may contain errors
Lab products found in correlation
Sl327, by Bio-Techne (1 mentions)
Acetylsalicylic acid, by Merck Group (1 mentions)
Bay 11 7085, by Merck Group (1 mentions)
Sb431542, by Bio-Techne (1 mentions)
Eplerenone, by Merck Group (1 mentions)
Aldosterone, by Merck Group (1 mentions)
L sulforaphane, by Cayman Chemical (1 mentions)
Tiron, by Santa Cruz Biotechnology (1 mentions)
Acetylcholine, by Merck Group (1 mentions)
Phenylephrine, by Merck Group (1 mentions)
Cell extraction buffer, by Thermo Fisher Scientific (1 mentions)
Bovine serum albumin (bsa), by Jackson ImmunoResearch (1 mentions)
Mouse anti gapdh monoclonal antibody, by Novus Biologicals (1 mentions)
Np40 cell lysis buffer, by Thermo Fisher Scientific (1 mentions)
Sb 203580 hydrochloride, by Bio-Techne (1 mentions)
Bay11 7082, by Merck Group (1 mentions)
7 protocols using sb239063
1
Ethanol and Inhibitor Preparation
2
Biomass-Induced Cytokine Signaling in Lung Fibroblasts
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To investigate the possible signaling pathways activated by biomass and resulting in cytokine production in primary human lung fibroblasts, inhibitors of the PI3 kinase, ERK, JNK, SMAD, p38 MAP kinase, NFκB, and COX pathways were used. The signaling pathway inhibitors were used at the following concentrations which have been shown to be specific and effective in human airway cells [29 (link),30 (link),31 (link),32 (link),33 (link)]—L294002 (3 μM), PD98059 (10 μM), SP600125 (10 μM) (Chalbiochem, San Diego, CA, USA), SB431542 (10 μM), SB239063 (3 μM) (Tocris, Ellisville, MO, USA), BAY117085 (10−3 μM), and acetylsalicylic acid (0.1 μM) (Sigma-Aldrich).
Signaling inhibitors were added to primary human lung fibroblasts for one hour prior to biomass smoke stimulation. A vehicle control (0.06% DMSO) was also used. Supernatant was collected after 24 h.
Signaling inhibitors were added to primary human lung fibroblasts for one hour prior to biomass smoke stimulation. A vehicle control (0.06% DMSO) was also used. Supernatant was collected after 24 h.
3
Aldosterone and Cardiovascular Effects
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Aldosterone, eplerenone, phenylephrine, and acetylcholine were purchased from Sigma-Aldrich (St. Louis, MO, USA). Tiron (Santa Cruz, Dallas, TX, USA), L-sulforaphane (Cayman, Ann Arbor, MI, USA), and SB 239063 (Tocris, Bristol, UK) were also purchased.
4
Aortic Diameter Measurement in CaCl2-Induced Mice
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In a separate CaCl2 model experiment, mice were further injected intraperitoneally with 1 mg/kg of SB239063 (a p38 inhibitor, Tocris bioscience), dissolved in 3% dimethylsulfoxide (DMSO, resolved with PBS) or vehicle only, at multiple time points, 1 h before CaCl2 application and thereafter daily for 6 week. At the indicated time intervals after the CaCl2 application, mice were sacrificed to measure the diameter of the aorta.
5
Kv2.1 Phosphorylation Signaling Protocol
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Primary antibodies used in this study were from the following sources: mouse anti-Kv2.1 monoclonal antibody (clone K89/34) and rabbit anti-Kv2.1 antibody were obtained from NeuroMab (Davis, CA) and Alomone Lab (Jerusalem, Israel), respectively; mouse anti-phosphotyrosine monoclonal antibody (PY99) was from Santa Cruz (Dallas, TX), and mouse anti-GAPDH monoclonal antibody was from Novus (Littleton, CO). SB239063 was purchased from Tocris (Ellisville, MO). An affinity-purified rabbit phospho-specific antibody raised against Kv2.1 residue S800 was described previously [21 (link)]. Cell Extraction Buffer and NP40 Cell Lysis Buffer were from Invitrogen (Camarillo, CA). Bovine serum albumin (BSA) was from Jackson ImmunoResearch (West Grove, PA), and bicinchoninic acid (BCA) based protein assay reagents were from Thermo Scientific (Rockford, IL). Unless specified, all other chemicals used were of analytical grade quality or better and were from Sigma-Aldrich (St. Louis, MO).
6
Cellular Responses to Replication Stress
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All treatments, including APH, HU, UV, ATRi, ATMi, p38i and CHK1i, were added into fresh ESC medium and the cells were kept at 37°C under 3% O2 tension overnight (16–17 hr) unless otherwise indicated. APH was used at concentrations ranging from 0.4 to 6 µM as indicated. Similarly, HU was used at 0.1 mM - 0.2 mM. ATMi (KU-55933) and ATRi (VE 822) were used at the concentrations of 10 µM and 1 µM respectively. The CHK1 inhibitors LY2603618 and UCN-01 were used at the concentrations of 200 nM and 100 nM, respectively. UV radiation exposure was performed at the dosage of 5 J/m2 or 10 J/m2. For induction of ETAA1-AAD expression, Dox was used at the concentration of 1 µg/mL for 48 hr. SB 203580 hydrochloride (Tocris Bioscience) and SB 239063 (Tocris Bioscience) were used at the concentration of 5 and 10 µM.
7
Inhibition of Inflammatory Pathways
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HPFs and BEAS-2Bs were treated with inhibitors of p38 MAPK (SB239063, 3µM, IC 50 = 44nM) (Tocris, Ellisville, MO, USA), JNK (SP600125, 10µM, IC 50 = 40 nM for JNK-1 and 2 and 90 nM for JNK-3) (Calbiochem, San Diego, CA), COX (indomethacin, 10µM, IC 50 = 0.23µM for COX-1 and IC 50 = 0.63 µM for COX-2) (Sigma) and NF-κB (BAY-117082, 10µM, IC 50 = 10µM) (Sigma) for 1 hour before stimulation with AA (100µM) with or without PolyI:C (10µg/mL) or LTA (10µg/mL).
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